After FLT3 binds to ligands, it will dimerize or autophosphorylate and activate JAK-STAT, PI3K, and MAPK signaling pathways, which can promote tumor cell proliferation and differentiation or inhibit tumor cell apoptosis.166 FLT3 is expressed in most AML patients and exists 30% mutations. The gene discussed is SOAT1; the disease is neoplasm.